ArticleThe Journal of biological chemistry2010
Helicobacter pylori induces ERK-dependent formation of a phospho-c-Fos c-Jun activator protein-1 complex that causes apoptosis in macrophages.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 90 citations in OpenAlex.
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Analysis of anticancer drug associated adverse reactions in depressive patients from vigibase.Scientific reports · 2025Article
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- A Narrative Review: Immunometabolic Interactions of Host-Gut Microbiota and Botanical Active Ingredients in Gastrointestinal Cancers.International journal of molecular sciences · 2024Review
- Current research on the interaction between Helicobacter pylori and macrophages.Molecular biology reports · 2024Review
- Strategies ofFrontiers in cellular and infection microbiology · 2024Review
- Apoptosis and its pathways as targets for intracellular pathogens to persist in cells.Parasitology research · 2023Review
- Immunohistochemical Characterization of M1, M2, and M4 Macrophages in Leprosy Skin Lesions.Pathogens (Basel, Switzerland) · 2023Article
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- Transcriptome analysis of PK-15 cells expressing CSFV NS4A.BMC veterinary research · 2022Article
- Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022Review
- Cystathionine γ-lyase exacerbates Helicobacter pylori immunopathogenesis by promoting macrophage metabolic remodeling and activation.JCI insight · 2022Article
- Transcriptome Analysis of Genes Responding to Infection of Leghorn Male Hepatocellular Cells With Fowl Adenovirus Serotype 4.Frontiers in veterinary science · 2022Article
- Article
- The role of polyamines in gastric cancer.Oncogene · 2021Review
- Polyamines and related signaling pathways in cancer.Cancer cell international · 2020Review
- Review
- HAging · 2019Article
- Resolution of Gastric Cancer-Promoting Inflammation: A Novel Strategy for Anti-cancer Therapy.Current topics in microbiology and immunology · 2019Review
- Cell Cycle Arrest and Apoptosis Induced by Porphyromonas gingivalis Require Jun N-Terminal Protein Kinase- and p53-Mediated p38 Activation in Human Trophoblasts.Infection and immunity · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Macrophages are essential components of innate immunity, and apoptosis of these cells impairs mucosal defense to microbes. Helicobacter pylori is a gastric pathogen that infects half of the world population and causes peptic ulcer disease and gastric cancer. The host inflammatory response fails to eradicate the organism. We have reported that H. pylori induces apoptosis of macrophages by generation of polyamines from ornithine decarboxylase (ODC), which is dependent on c-Myc as a transcriptional enhancer. We have now demonstrated that expression of c-Myc requires phosphorylation and nuclear translocation of ERK, which results in phosphorylation of c-Fos and formation of a specific activator protein (AP)-1 complex. Electromobility shift assay and immunoprecipitation revealed a previously unrecognized complex of phospho-c-Fos (pc-Fos) and c-Jun in the nucleus. Fluorescence resonance energy transfer demonstrated the interaction of pc-Fos and c-Jun. The capacity of this AP-1 complex to bind to putative AP-1 sequences was demonstrated by oligonucleotide pulldown and fluorescence polarization. Binding of the pc-Fos.c-Jun complex to the c-Myc promoter was demonstrated by chromatin immunoprecipitation. A dominant-negative c-Fos inhibited H. pylori-induced expression of c-Myc and ODC and apoptosis. H. pylori infection of mice induced a rapid infiltration of macrophages into the stomach. Concomitant apoptosis depleted these cells, and this was associated with formation of a pc-Fos.c-Jun complex. Treatment of mice with an inhibitor of ERK phosphorylation attenuated phosphorylation of c-Fos, expression of ODC, and apoptosis in gastric macrophages. A unique AP-1 complex in gastric macrophages contributes to the immune escape of H. pylori.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.